Cardiac valve endothelial cells: Relevance in the long-term function of biologic valve prostheses

Simon, Andrè; Wilhelmia, M.; Steinhoff, Gustav; Harringer, Wolfgang; Brücke, P; Haverich, Axel

doi:10.1016/s0022-5223(98)70167-9

Cited by 21 publications

(22 citation statements)

References 27 publications

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“…Endothelial staining by vWF was graded as follows: no staining (0), single-cell positivity (1), nonconfluent positivity (2), and confluent endothelial positivity (3). Staining of myofibroblast immigration by ␣-actin and procollagen I was rated as follows: no staining (0), single-cell positivity (1), incomplete positivity in patchy areas (2), and complete positivity throughout leaflet (3). encouraging, these preliminary results of viable valve regeneration after tissue engineering leave a number of questions to be addressed.…”

Section: Discussionmentioning

confidence: 99%

“…1 This may partially be due to their immunogenic potential or due to detergent fixation leading to the inability to be repopulated by autologous cells. 2 The fact that the current biological heart valve prostheses do not allow the reconstitution of viable heart valve tissue may be a major factor influencing thrombogenicity, inflammation, and limitation of long-term durability.…”

mentioning

confidence: 99%

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Tissue Engineering of Pulmonary Heart Valves on Allogenic Acellular Matrix Conduits : In Vivo Restoration of Valve Tissue

Steinhoff

Stock²,

Karim³

et al. 2000

Circulation

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277

231

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Background-Tissue engineering using in vitro-cultivated autologous vascular wall cells is a new approach to biological heart valve replacement. In the present study, we analyzed a new concept to process allogenic acellular matrix scaffolds of pulmonary heart valves after in vitro seeding with the use of autologous cells in a sheep model. Methods and Results-Allogenic heart valve conduits were acellularized by a 48-hour trypsin/EDTA incubation to extract endothelial cells and myofibroblasts. The acellularization procedure resulted in an almost complete removal of cells.After that procedure, a static reseeding of the upper surface of the valve was performed sequentially with autologous myofibroblasts for 6 days and endothelial cells for 2 days, resulting in a patchy cellular restitution on the valve surface.The in vivo function was tested in a sheep model of orthotopic pulmonary valve conduit transplantation. Three of 4 unseeded control valves and 5 of 6 tissue-engineered valves showed normal function up to 3 months. Unseeded allogenic acellular control valves showed partial degeneration (2 of 4 valves) and no interstitial valve tissue reconstitution. Tissue-engineered valves showed complete histological restitution of valve tissue and confluent endothelial surface coverage in all cases. Immunohistological analysis revealed cellular reconstitution of endothelial cells (von Willebrand factor), myofibroblasts (␣-actin), and matrix synthesis (procollagen I). There were histological signs of inflammatory reactions to subvalvar muscle leading to calcifications, but these were not found in valve and pulmonary artery tissue. Conclusions-The in vitro tissue-engineering approach using acellular matrix conduits leads to the in vivo reconstitution of viable heart valve tissue.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Tissue Engineering of Pulmonary Heart Valves on Allogenic Acellular Matrix Conduits : In Vivo Restoration of Valve Tissue

Steinhoff

Stock²,

Karim³

et al. 2000

Circulation

Self Cite

277

231

View full text Add to dashboard Cite

show abstract

“…For immunohistochemical examination, samples were cut into 3-5 mm sections and stored at K20 8C until staining. Due to temperature-dependent antibody kinetics, a slightly modified alkaline phosphatase/anti alkaline phosphatase (APAAP) staining method previously described elsewhere was applied [5]. Negative and positive controls were performed in parallel to all staining series and found valid in all cases.…”

Section: Methodsmentioning

confidence: 99%

Upregulation of endothelial adhesion molecules in hearts with congestive and ischemic cardiomyopathy: immunohistochemical evaluation of inflammatory endothelial cell activation

Wilhelmi

Leyh

Wilhelmi

et al. 2005

European Journal of Cardio-Thoracic Surgery

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“…Colocalization of mAb 10G with anti-CD31 antibody confirmed the binding of mAb 10G but not mAb 9C to mouse heart endothelial cells (Figure 2e). As the expression of CD31 is restricted to endothelial cells, 42 the mouse heart valve was stained for expression of CD31 antigens revealing the endothelial lining. Furthermore, we found IgG and complement C3 deposits on the valves of mice intravenously immunized with mAb 10G, but not in those of mice treated with mAb 9C (Figure 3a and b).…”

Section: Resultsmentioning

confidence: 99%

Molecular mimicry between streptococcal pyrogenic exotoxin B and endothelial cells

Luo

Chuang

et al. 2010

Laboratory Investigation

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Molecular mimicry between group A streptococcus and host antigens has important roles in the development of poststreptococcal sequelae, including glomerulonephritis and rheumatic heart disease (RHD). The etiology of RHD involves host cross-reactivity with M proteins and carbohydrate antigens. In this study, we show that anti-streptococcal pyrogenic exotoxin B (SPE B) antibodies exhibited characteristics of autoantibodies, which cross-react with endothelial cells. Immunoglobulin G (IgG) deposition and complement activation were observed in the heart valve of SPE B-immunized mice. In addition, apoptosis in the heart valve was detected in SPE B-immunized mice. An anti-SPE B monoclonal antibody (mAb) 10G showed cross-reactivity with human microvascular endothelial (HMEC-1) cells and mouse valve endothelial cells. Passive immunization with mAb 10G also caused IgG deposition, complement activation, and apoptotic cell death in the mouse heart valve. We conducted peptide array and ELISA using synthetic peptides to identify the SPE B antigenic epitope recognized by mAb 10G. Results showed that the major epitope of mAb 10G is localized to amino-acid residues 296-310 of SPE B (P7-8). The cross-reactivity of mAb 10G with endothelial cells was inhibited using P7-8 peptides for competition. These results suggest that anti-SPE B antibodies cross-react with endothelial cells, and that a dominant epitope is located within the amino-acid residues 296-310 of SPE B. Moreover, we found that mAb 10G can also bind to N-acetyl-b-D-glucosamine (GlcNAc) conjugated with bovine serum albumin (BSA), but not to BSA or M1 protein.Competition assay showed that the binding activity of mAb 10G with GlcNAc-BSA and P7-8 of SPE B was inhibited by pretreatment with GlcNAc-BSA or P7-8 peptides. Therefore, our results suggest that conformational molecular mimicry may exist between SPE B and GlcNAc.

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Cardiac valve endothelial cells: Relevance in the long-term function of biologic valve prostheses

Abstract: Inasmuch as valves from previously transplanted hearts seem to be free from degeneration, we conclude that reduction of the immunogenicity of allograft valve prostheses by HLA matching or immunosuppressive treatment might further improve long-term results after allograft valve replacement.

Cited by 21 publications

References 27 publications

Tissue Engineering of Pulmonary Heart Valves on Allogenic Acellular Matrix Conduits : In Vivo Restoration of Valve Tissue

Tissue Engineering of Pulmonary Heart Valves on Allogenic Acellular Matrix Conduits : In Vivo Restoration of Valve Tissue

Upregulation of endothelial adhesion molecules in hearts with congestive and ischemic cardiomyopathy: immunohistochemical evaluation of inflammatory endothelial cell activation

Molecular mimicry between streptococcal pyrogenic exotoxin B and endothelial cells

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